KRAS audio was popular in the tumors but only within a single cell line, SKOV 8. SKOV 8 cells did show high levels of RAS GTP and were MEK dependent, and their reaction to MEK and AKT inhibitors was just like those of the OVCAR 5 cell line, which conveys Daclatasvir HCV protease inhibitor a KRAS G12V allele, a mutation present in less than hundreds of serous ovarian cancers. Variations between KRAS amplification and mutation, however, could become clear with further study and thus it would be inappropriate to consider OVCAR 5 as a representative design for the larger cohort of RAS altered ovarian tumors, most of which exhibit amplification of wild type KRAS. In conclusion, the data suggest that the currently available ovarian cancer cell lines only slightly reflect the complexity of the human condition and that a richer panel of ovarian cancer cell lines with multiple representative examples based on each genetic class becomes necessary. Our built-in evaluation of the cell line and growth section also illustrates the problem of using selection based copy number information to recognize these patients with functional gene amplifications and deletions. Cellular differentiation In case of PTEN, content number position as scored by both the GISTIC or RAE calculations correlated highly with PTEN mRNA expression. More, PTEN copynumber basic or homozygous deletion calls were good predictors of the presence or loss in PTEN protein and quantities of p AKT expression by immunohistochemistry and reverse phase protein arrays. But, hemizygous loss of the PTEN gene did not easily correlate with practical loss of PTEN protein expression by IHC or down-regulation of PTEN mRNA expression. These suggest that in lack of homozygous deletion, copy number information alone was insufficient to accurately define PTEN status. A heterogeneous buy Apremilast sample of PTEN expression by IHC was also common suggesting that clonal heterogeneity will end up being yet another problem to the use of array based platforms to properly identify tumors with functional loss in PTEN. In summary, our data suggest that the game of AKT inhibitors will be limited to tumors harboring genomic adjustments inside the pathway and that combination therapy will have to elicit a tumefaction response or regression in many tumors. On the foundation of those data, we predict a low response rate with selective AKT route inhibitors when such agents are used alone in ovarian cancers. This fact may necessitate the development of such compounds initially in cohorts of individuals from other growth lineages when the frequency of defined PI3K/AKT path changes is large.